imported>S |
imported>Doyeon Kwak |
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| − | <p><span style="font-size: small">Telomeres, the protective elements at the ends of<br />
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| − | chromosomes, need to be maintained for cells to<br />
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| − | proliferate indefinitely. In many human cancers, the<br />
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| − | telomeric DNA is replenished by telomerase. However, a<br />
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| − | second pathway for telomere maintenance, referred to as<br />
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| − | the ALT pathway, has increasingly been recognized in<br />
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| − | human cancers. The genetic basis for activation of ALT is<br />
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| − | not known, but recent data have implicated a chromatin<br />
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| − | remodeling complex (ATRX/DAXX) and the histone variant<br />
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| − | H3.3 as players in the repression of ALT. We have<br />
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| − | examined a large panel of ALT cell lines for their genetic<br />
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| − | and cell biological features and found that loss of ATRX is a<br />
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| − | common event in the genesis of ALT lines. In addition, we<br />
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| − | document that ALT cell lines frequently undergo chromosomal<br />
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| − | changes and are impaired in their ability to detect<br />
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| − | and repair damage in their DNA. These hallmarks of ALT<br />
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| − | are expected to facilitate the detection of ALT–type tumors<br />
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| − | in the clinic and may lead to ALT–specific treatments.</span></p>
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